Cerebral edema is characterised as being an excessive accumulation of water in the intra- and/or extracellular compartments of the brain (Pollay (1996) In Neurosurgery, 2nd ed. Mc Graw Hill Book Co., New York, 335-344). Cerebral edema may be of neurological origin, as in the cases of ischaemic attacks, intracerebral haemorrhages, brain tumours, cases of meningitis or of encephalitis, or of non-neurological origin, as in cases of diabetic ketoacidosis, lactic acidosis, hypertensive encephalopathy, malignant hypertension, hyponatraemia or an effect of high altitude.
The principal consequence of cerebral edema is an increase in the intracranial fluid pressure, leading to a reduction in the blood supply to the brain and the partial or total destruction of insufficiently vascularized cerebral tissues.
Few compounds are available for the pharmacological treatment of cerebral edemas, and among the most commonly used the following compounds may be mentioned:                mannitol, and to a lesser degree glycerol, are used as agents for osmotherapy; however, prolonged administration of mannitol leads to an electrolytic imbalance which can counterbalance its beneficial effects by causing for example cardiopulmonary troubles (Davis et al. (1994) J. Neurosci. Nurs. 26:170-174);        diuretics, such as furosemide, are only used in controlled release to prolong the effect of the osmotic agents;        corticoids, particularly glucocorticoids, such as dexamethasone, act principally on the blood vessels and are therefore particularly indicated in the case of cerebral edemas of vascular origin; on the other hand they are nor recommended in the treatment of edemas following ischaemias or haemorrhages; moreover, systemic complications associated with steroids can lead to a deterioration of the patient's condition (Rosenberg (2000) In Neurology in clinical practice, 3rd ed. Butterworth Heinmann, Boston, 2:1545-1559);        barbiturates, less used than in the past, seem to act by causing a decrease in the level of metabolic activity; however, these compounds also cause systemic hypotension and pulmonary insufficiencies.        
Moclobemide is a benzamide derivative which inhibits type A monoamine oxidase in a reversible manner and which is currently used as an antidepressant. Few undesirable side effects following its use are documented.

The synthesis of this compound and of certain of its derivatives is described in the U.S. Pat. No. 4,210,754. Moreover, numerous metabolites of moclobemide have been identified (Jauch et al. (1990) Acta Psychiatr. Sand. Suppl. 360:87-90); these metabolites are characterised in particular by a hydroxylation of the phenyl group or by C or N oxidations of the morpholine group.